Allsopp T E, Fazakerley J K
Fujisawa Institute of Neuroscience in Edinburgh, Dept of Neuroscience, University of Edinburgh, UK.
Trends Neurosci. 2000 Jul;23(7):284-90. doi: 10.1016/s0166-2236(00)01591-5.
Depending on their differentiation state, vertebrate neurones can commit suicide after neurotropic virus infection. Such suicide might be an evolved strategy in multicellular organisms for limiting virus expansion. Regulation of suicide in this context operates by a programme similar to that activated during embryogenesis or in response to nervous-system injury and disease. In contrast to immature neurones that can readily initiate apoptosis following infection, mature neurones are generally highly resistant and can survive for long periods if they remain functional. Mature, infected neurones might gain competence to die owing to the attuned activation of pathways that sensitize the cell to subsequent stress. The consequence of either perturbation of function as a result of viral persistence or a chronic but progressive loss of infected neurones might be a failure of key neural functions.
脊椎动物神经元可根据其分化状态在嗜神经病毒感染后自杀。这种自杀可能是多细胞生物中限制病毒扩散的一种进化策略。在这种情况下，自杀的调控通过一个类似于胚胎发育过程中或对神经系统损伤和疾病作出反应时激活的程序来运作。与感染后能轻易启动凋亡的未成熟神经元不同，成熟神经元通常具有高度抗性，并且如果它们保持功能，可以长期存活。成熟的受感染神经元可能由于使细胞对后续应激敏感的途径的协调激活而获得死亡能力。病毒持续存在导致的功能紊乱或受感染神经元的慢性但渐进性丧失的后果可能是关键神经功能的丧失。
